Eksp Klin Farmakol. 2010 Dec;73(12):2-5.[On the mechanism of noopept action: decrease in activity of stress-induced kinases and increase in expression of neutrophines].[Article in Russian]Ostrovskaia RU, Vakhitova IuV, Salimgareeva MKh, Iamidanov RS, Sadovnikov SV, Kapitsa IG, Seredenin SB.AbstractThe influence of noopept (N-phenylacetyl-L-prolylglycine ethyl ester, GVS-111)--a drug combining the nootrope and neuroprotector properties--on the activity of mitogen-activated protein kinases (MAPKs) and the level of NGF and BDNF gene and protein expression in the frontal cortex, hippocampus, and hypothalamus has been studied in rats. Under conditions of chronic administration (28 days, 0.5 mg/day, i.p.), noopept decreased the activity of stress-induced kinases (SAPK/JNK 46/54 and pERK1/2) in rat hippocampus and increases the level of mRNA of the BDNF gene in both hypothalamus and hippocampus. The content of BDNF protein in the hypothalamus was also somewhat increased. In the context of notions about the activation of stress-induced kinases, as an important factor of amyloidogenesis and tau-protein deposition in brain tissue, and the role of deficiency of the neurotrophic factors in the development of neurodegenerative processes, the observed decrease in the activity of stress-activated MAPKs and increased expression of BDNF as a result of noopept administration suggest thatthis drug hasaspecific activity withrespect to some pathogenetic mechanisms involved in the Alzheimer disease.PMID: 21395007 [PubMed - indexed for MEDLINE]

Eksp Klin Farmakol. 2010 Jan;73(1):2-6.[Effect of the novel nootropic and neuroprotective dipeptide noopept on the streptozotocin-induced model of sporadic Alzheimer disease in rats].[Article in Russian]Ostrovskaia RU, Tsaplina AP, Vakhitova IuV, Salimgareeva MKh, Iamidanov RS.AbstractStreptozotocin-intracerebroventricularly treated rats are proposed as an experimental model of sporadic Alzheimer disease (AD). Diabetogenic toxin streptozotocin (STZ) administered in both cerebral ventricles in a dose of 3 mg/kg decreases the expression of NGF and BDNF mainly in the hippocampus and increases the content of malonic dialdehyde (MDA)--a product of lipid peroxidation--in the brain tissues. These metabolic changes are accompanied by a pronounced cognitive deficiency, which is manifested by long-term memory deterioration in the passive avoidance test. These manifestations of pathology are not accompanied by hyperglycemia in the case of intraventricular STZ administration, in contrast to the systemic (in particular, intraperitoneal) route of introduction that causes a pronounced increase in the blood glucose level. These results are consistent with the existing notions that (i) STZ administered intraventricularly provokes a complex of changes imitating the sporadic AD and (ii) this disease can be considered as a manifestation of type-III diabetes. The new original cognition enhancing and neuroprotective dipeptide noopept decreases the aforementioned metabolic changes and the accompanying long-term deterioration of the memory. Previously, this systemically active dipeptide was shown to be capable of increasing expression of NGF and BDNF in the hippocampus, stimulating the antibody production to beta-amyloid, inhibiting the lipid peroxidation, activating the endogenous antioxidant systems, and decreasing the rate of glutamate release (cholinopositive effect). Taken together, these data indicate that noopept can be considered as a multipotent substance acting upon several important pathogenic chainsof the sporadic AD.PMID: 20184279 [PubMed - indexed for MEDLINE]

Eksp Klin Farmakol. 2010 Dec;73(12):2-5.[On the mechanism of noopept action: decrease in activity of stress-induced kinases and increase in expression of neutrophines].[Article in Russian]Ostrovskaia RU, Vakhitova IuV, Salimgareeva MKh, Iamidanov RS, Sadovnikov SV, Kapitsa IG, Seredenin SB.AbstractThe influence of noopept (N-phenylacetyl-L-prolylglycine ethyl ester, GVS-111)--a drug combining the nootrope and neuroprotector properties--on the activity of mitogen-activated protein kinases (MAPKs) and the level of NGF and BDNF gene and protein expression in the frontal cortex, hippocampus, and hypothalamus has been studied in rats. Under conditions of chronic administration (28 days, 0.5 mg/day, i.p.), noopept decreased the activity of stress-induced kinases (SAPK/JNK 46/54 and pERK1/2) in rat hippocampus and increases the level of mRNA of the BDNF gene in both hypothalamus and hippocampus. The content of BDNF protein in the hypothalamus was also somewhat increased. In the context of notions about the activation of stress-induced kinases, as an important factor of amyloidogenesis and tau-protein deposition in brain tissue, and the role of deficiency of the neurotrophic factors in the development of neurodegenerative processes, the observed decrease in the activity of stress-activated MAPKs and increased expression of BDNF as a result of noopept administration suggest thatthis drug hasaspecific activity withrespect to some pathogenetic mechanisms involved in the Alzheimer disease.PMID: 21395007 [PubMed - indexed for MEDLINE]

Eksp Klin Farmakol. 2010 Jan;73(1):2-6.[Effect of the novel nootropic and neuroprotective dipeptide noopept on the streptozotocin-induced model of sporadic Alzheimer disease in rats].[Article in Russian]Ostrovskaia RU, Tsaplina AP, Vakhitova IuV, Salimgareeva MKh, Iamidanov RS.AbstractStreptozotocin-intracerebroventricularly treated rats are proposed as an experimental model of sporadic Alzheimer disease (AD). Diabetogenic toxin streptozotocin (STZ) administered in both cerebral ventricles in a dose of 3 mg/kg decreases the expression of NGF and BDNF mainly in the hippocampus and increases the content of malonic dialdehyde (MDA)--a product of lipid peroxidation--in the brain tissues. These metabolic changes are accompanied by a pronounced cognitive deficiency, which is manifested by long-term memory deterioration in the passive avoidance test. These manifestations of pathology are not accompanied by hyperglycemia in the case of intraventricular STZ administration, in contrast to the systemic (in particular, intraperitoneal) route of introduction that causes a pronounced increase in the blood glucose level. These results are consistent with the existing notions that (i) STZ administered intraventricularly provokes a complex of changes imitating the sporadic AD and (ii) this disease can be considered as a manifestation of type-III diabetes. The new original cognition enhancing and neuroprotective dipeptide noopept decreases the aforementioned metabolic changes and the accompanying long-term deterioration of the memory. Previously, this systemically active dipeptide was shown to be capable of increasing expression of NGF and BDNF in the hippocampus, stimulating the antibody production to beta-amyloid, inhibiting the lipid peroxidation, activating the endogenous antioxidant systems, and decreasing the rate of glutamate release (cholinopositive effect). Taken together, these data indicate that noopept can be considered as a multipotent substance acting upon several important pathogenic chainsof the sporadic AD.PMID: 20184279 [PubMed - indexed for MEDLINE]

All of them are from Europe with three in Russian. My concern with Noopept wasn't it's cognitive enhancement but the possibility that the 1000x potency claim was over-exaggerated. Thank you for those abstracts!

Hmm interesting, I have not looked into noopept before. I have had my eyes set on a similar nootropic that only seems to exist in Russia, Phenylpiracetam (phenotropyl). Aaaah why can't these be available in the US and not just hiding out in Russia!?

I do not recommend going by strength ratings alone. With the existing racetams, they are proclaimed to be "X times stronger than piracetam." I do not know how this 'strength' is estimated, but the effects of each are very different from one another, and that is really what makes the difference. I would recommend ordering some and trying it; that is the best evidence you will get!

I believe it simply means that the effective dosage is 1000x, approximately, since the normal dosage of noopept is 10-30mg per day whereas the normal dosage of piracetam is 3-9g per day. It is not in reference to the effects of the substances, AFAIK. Although user reports do indicate that noopept is noticeably better or more effective than piracetam. Can anyone confirm or deny my assumption?

@bzyzny - I just finished my 3 month trial with noopept. I initially (3 weeks) replaced my piracetam with noopept after a one week washout. Initial results were positive but subtle: elevated energy, good focus, pretty much par with piracetam. However, contrary to the wikipedia entry I noticed a marked increase in irritability towards others (specifically) and situations (in general). I also noticed jittery-ness after my 3rd 10mg dose of the day. After 3 weeks of using just noopept I opted to reintroduce piracetam in my stack. I think the two synergize well initially but the noopept seemed to "fade" after a while.

YMMV, but for me noopept won't be part of my regular rotation. I tossed the remainder...piracetam is so darn cheap and so well tolerated

I believe it simply means that the effective dosage is 1000x, approximately, since the normal dosage of noopept is 10-30mg per day whereas the normal dosage of piracetam is 3-9g per day. It is not in reference to the effects of the substances, AFAIK. Although user reports do indicate that noopept is noticeably better or more effective than piracetam. Can anyone confirm or deny my assumption?

This is what I always believed as well. It's not that noopept will make your memory or focus x1000 better, but rather you only need 1/1000 the amount. And as far as which is better, I think a lot depends on your personal brain chemistry (and also what you're trying to accomplish). I know people who much prefer noopept over piracetam, and almost as many that go the other way.